Evidence from studies on postmenopausal osteoporosis suggests that estrogen deficiency induces a persistent pro-inflammatory state, significantly increasing the secretion of inflammatory mediators within the local microenvironment, including interleukins (ILs), tumor necrosis factor-alpha (TNF-α), IL-1β, as well as reactive oxygen species (ROS) (12, 36, 37). The gene discussed is IL1B; the disease is postmenopausal osteoporosis.